Collaborators NCDC. NCD Countdown 2030: worldwide trends in non-communicable disease mortality and progress towards sustainable development goal target 3.4. Lancet. 2018;392(10152):1072–88.
Fabiani I, Chianca M, Aimo A, et al. Use of new and emerging cancer drugs: what the cardiologist needs to know. Eur Heart J. 2024;45(22):1971–87.
Mattioli R, Ilari A, Colotti B, et al. Doxorubicin and other anthracyclines in cancers: activity, chemoresistance and its overcoming. Mol Aspects Med. 2023;93:101205.
Article CAS PubMed Google Scholar
McGowan JV, Chung R, Maulik A, et al. Anthracycline chemotherapy and cardiotoxicity. Cardiovasc Drugs Ther. 2017;31(1):63–75.
Article CAS PubMed PubMed Central Google Scholar
Gradishar WJ, Moran MS, Abraham J, et al. Breast cancer, version 4.2021. J Natl Compr Canc Ne. 2021;19(5):485–94.
Farías JG, Molina VM, Carrasco RA, et al. Antioxidant therapeutic strategies for cardiovascular conditions associated with oxidative stress. Nutrients. 2017;9(9):966.
Article PubMed PubMed Central Google Scholar
Narezkina A, Narayan HK, Zemljic-Harpf AE. Molecular mechanisms of anthracycline cardiovascular toxicity. Clin Sci (Lond). 2021;135(10):1311–32.
Davies KJ, Doroshow JH. Redox cycling of anthracyclines by cardiac mitochondria. I. Anthracycline radical formation by NADH dehydrogenase. J Biol Chem. 1986;261(7):3060–7.
Article CAS PubMed Google Scholar
Doroshow JH, Davies KJ. Redox cycling of anthracyclines by cardiac mitochondria. II. Formation of superoxide anion, hydrogen peroxide, and hydroxyl radical. J Biol Chem. 1986;261(7):3068–74.
Article CAS PubMed Google Scholar
Zhao Y, McLaughlin D, Robinson E, et al. Nox2 NADPH oxidase promotes pathologic cardiac remodeling associated with doxorubicin chemotherapy. Cancer Res. 2010;70(22):9287–97.
Article CAS PubMed PubMed Central Google Scholar
Vermot A, Petit-Härtlein I, Smith SME, et al. NADPH Oxidases (NOX): An overview from discovery, molecular mechanisms to physiology and pathology. Antioxidants (Basel). 2021;10(6):890.
Article CAS PubMed PubMed Central Google Scholar
Prosser BL, Ward CW, Lederer WJ. X-ROS signaling: rapid mechano-chemo transduction in heart. Science. 2011;333(6048):1440–5.
Article CAS PubMed Google Scholar
Elnakish MT, Hassanain HH, Janssen PM, et al. Emerging role of oxidative stress in metabolic syndrome and cardiovascular diseases: important role of Rac/NADPH oxidase. J Pathol. 2013;231(3):290–300.
Article CAS PubMed Google Scholar
Octavia Y, Tocchetti CG, Gabrielson KL, et al. Doxorubicin-induced cardiomyopathy: from molecular mechanisms to therapeutic strategies. J Mol Cell Cardiol. 2012;52(6):1213–25.
Article CAS PubMed Google Scholar
Wojnowski L, Kulle B, Schirmer M, et al. NAD(P)H oxidase and multidrug resistance protein genetic polymorphisms are associated with doxorubicin-induced cardiotoxicity. Circulation. 2005;112(24):3754–62.
Article CAS PubMed Google Scholar
Deng S, Kruger A, Kleschyov AL, et al. Gp91phox-containing NAD(P)H oxidase increases superoxide formation by doxorubicin and NADPH. Free Radic Biol Med. 2007;42(4):466–73.
Article CAS PubMed Google Scholar
Roy R, Wilcox J, Webb AJ, et al. Dysfunctional and dysregulated nitric oxide synthases in cardiovascular disease: Mechanisms and therapeutic potential. Int J Mol Sci. 2023;24(20):15200.
Article CAS PubMed PubMed Central Google Scholar
Mukhopadhyay P, Rajesh M, Batkai S, et al. Role of superoxide, nitric oxide, and peroxynitrite in doxorubicin-induced cell death in vivo and in vitro. Am J Physiol Heart Circ Physiol. 2009;296(5):H1466–83.
Article CAS PubMed PubMed Central Google Scholar
Vasquez-Vivar J, Martasek P, Hogg N, et al. Endothelial nitric oxide synthase-dependent superoxide generation from adriamycin. Biochemistry. 1997;36(38):11293–7.
Article CAS PubMed Google Scholar
Kalivendi SV, Kotamraju S, Zhao H, et al. Doxorubicin-induced apoptosis is associated with increased transcription of endothelial nitric-oxide synthase. Effect of antiapoptotic antioxidants and calcium. J Biol Chem. 2001;276(50):47266–76.
Article CAS PubMed Google Scholar
Wu S, Ko YS, Teng MS, et al. Adriamycin-induced cardiomyocyte and endothelial cell apoptosis: in vitro and in vivo studies. J Mol Cell Cardiol. 2002;34(12):1595–607.
Article CAS PubMed Google Scholar
Duquaine D, Hirsch GA, Chakrabarti A, et al. Rapid-onset endothelial dysfunction with adriamycin: evidence for a dysfunctional nitric oxide synthase. Vasc Med. 2003;8(2):101–7.
Finkelman BS, Putt M, Wang T, et al. Arginine-nitric oxide metabolites and cardiac dysfunction in patients with breast cancer. J Am Coll Cardiol. 2017;70(2):152–62.
Article CAS PubMed PubMed Central Google Scholar
Tadokoro T, Ikeda M, Ide T, et al. Mitochondria-dependent ferroptosis plays a pivotal role in doxorubicin cardiotoxicity. JCI Insight. 2020;5(9):e132747.
Article PubMed PubMed Central Google Scholar
Myers CE, McGuire WP, Liss RH, et al. Adriamycin: the role of lipid peroxidation in cardiac toxicity and tumor response. Science. 1977;197(4299):165–7.
Article CAS PubMed Google Scholar
Zhong H, Yin H. Role of lipid peroxidation derived 4-hydroxynonenal (4-HNE) in cancer: focusing on mitochondria. Redox Biol. 2015;4:193–9.
Article CAS PubMed Google Scholar
Ichikawa Y, Ghanefar M, Bayeva M, et al. Cardiotoxicity of doxorubicin is mediated through mitochondrial iron accumulation. J Clin Invest. 2014;124(2):617–30.
Article CAS PubMed PubMed Central Google Scholar
Menon AV, Kim J. Iron promotes cardiac doxorubicin retention and toxicity through downregulation of the mitochondrial exporter ABCB8. Front Pharmacol. 2022;13:817951.
Article CAS PubMed PubMed Central Google Scholar
Ikeda S, Matsushima S, Okabe K, et al. Blockade of L-type Ca(2+) channel attenuates doxorubicin-induced cardiomyopathy via suppression of CaMKII-NF-kappaB pathway. Sci Rep. 2019;9(1):9850.
Article PubMed PubMed Central Google Scholar
Kalivendi SV, Konorev EA, Cunningham S, et al. Doxorubicin activates nuclear factor of activated T-lymphocytes and Fas ligand transcription: role of mitochondrial reactive oxygen species and calcium. Biochem J. 2005;389(Pt 2):527–39.
Article CAS PubMed PubMed Central Google Scholar
Tscheschner H, Meinhardt E, Schlegel P, et al. CaMKII activation participates in doxorubicin cardiotoxicity and is attenuated by moderate GRP78 overexpression. PLoS ONE. 2019;14(4):e0215992.
留言 (0)